Neonatal lipid absorption is in part, dependent on the capacity of the liver and intestine to synthesize, excrete, and conserve bile acid. Preliminary studies performed in this laboratory have suggested that neonatal bile acid turnover is deficient, and that this may be a contributory factor in the development of steatorrhea in formula fed premature infants. Studies have, therefore, been undertaken to characterize the state of preparedness of the bile salt related activities of the liver and intestine just before birth. For this purpose fetal dogs and monkeys will be prepared in utero with vascular, intestinal, and biliary catheters. C14- and H3- labeled bile salts and bile salt precursors will be administered intravenously or into the intestine and the appearance of these materials in fetal plasma, liver, bile and other fetal tissues will be determined. Fetal to maternal placental transfer will also be measured by techniques available in the laboratory. The results have already established that bile salt turnover in the dog fetus closely resembles that in the adult, while the primate fetus' mechanisms are grossly deficient. Primate fetal hepatic excretion is reduced while placental transfer is increased in the primate fetus. It would thus appear that mechanisms for hepatic bile salt turnover, like those for bilirubin, are "maturing" during the perinatal period, and that deficiencies in these mechanisms are reflected in deficiencies of neonatal nutritive function.